AEBP1 Promotes Glioblastoma Progression and Activates the Classical NF-κB Pathway

Abstract

Objective. Our study was aimed at investigating the mechanistic consequences of the upregulation of adipocyte enhancer-binding protein 1 (AEBP1) in glioblastoma (GBM). Methods. The expression of AEBP1 in GBM was assessed by bioinformatics analysis and qRT-PCR; the effects of AEBP1 on GBM cell proliferation, migration, invasion, and tumor growth in vitro and in vivo were detected by a CCK-8 assay, colony formation assay, scratch assay, Transwell assay, and subcutaneous tumor formation, respectively. The activation of related signaling pathways was monitored using western blot. Results. Tumor-related databases and bioinformatics analysis revealed that AEBP1 was highly expressed in GBM and indicated poor outcome of patients; its high expression that was also confirmed in GBM tissues and cell lines was closely related to the tumor size. The results of in vitro experiments showed that AEBP1 could significantly promote GBM cell proliferation, migration, and invasion; in vivo experiments suggested that AEBP1 could contribute to the growth of GBM tumors. AEBP1 could upregulate the level of IκBα phosphorylation, decrease IκBα expression, activate the NF-κB signaling pathway, and promote the expression of downstream oncogenes. Conclusion. Upregulated AEBP1 in GBM promotes GBM cell proliferation, migration, and invasion and facilitates tumor growth in vivo by activating the classical NF-κB pathway.

AEBP1 Predicts Clinical Prognosis and is Associated with Immunocyte Infiltration in Gastric Cancer

“…Adipocyte enhancer binding protein 1 (AEBP1) was rst found in adipocytes and has been reported to be involved in multiple biological processes, including cholesterol homeostasis and in ammation [29], adipogenesis [30], cell differentiation [31]. It is found that AEBP1 can promote the occurrence and development of tumors [32][33][34]. We found that AEBP1 is upregulated in CRC, which is the same as the results of previous studies [34,35].…”

GRIK1 promotes glioblastoma malignancy and is a novel prognostic factor of poor prognosis

“…The Matrigel-Transwell invasion assay, colony formation investigations, and wound healing assays all demonstrated that the capacity of GBM cells to invade was greatly reduced when GRIK1 was inhibited. The molecular mechanisms of GBM growth and invasion are extremely complex and include many factors, such as lactate dehydrogenases [ 36 ], mitogen-activated protein kinase kinase kinase 1(MAP3K1)/c-JUN signaling-axis [ 37 ], Hsa_circ_0072309 [ 38 ], RNA-binding motif protein 8A (RBM8A) [ 9 ], LINC01711 [ 10 ],COL1A2 [ 11 ], adipocyte enhancer-binding protein 1 (AEBP1) [ 39 ], Nucleobindin-2 [ 40 ], the cross-talk between Notch1 signaling and CXCL12/CXCR4 system [ 41 ], PRL1/USP36/Snail2 axis [ 42 ], Zinc finger CCCH-type containing 15 (ZC3H15) [ 43 ], circ_0060055 [ 44 ], and Rhoj/Rac1/PAK signaling [ 45 ], etc.…”

Deciphering the Dose-Dependent Effects of Thymoquinone on Transcriptomic Changes and Cellular Proliferation in Glioblastoma

“…DNER, a noncanonical Notch ligand, was found to suppress glioma growth by inhibiting the oncogene TOR4A [72] and hindered the growth and induced differentiation of GBM-derived neurospheres [73]. Conversely, TQ treatment resulted in the downregulation of several genes overexpressed in GBM cells, including potential oncogenes like AEBP1, MIAT, GHR, LMO1, ELF3 [74][75][76][77][78], and genes involved in tumor proliferation and migration such as EPHA4, COL3A1, PCDH10, ROBO1, ADAMTS5, PCDH18, ST8SIA1 [79][80][81][82][83][84]. Additionally, TQ significantly downregulated genes associated with poor GBM prognosis, including PCSK5, KCNC1, MXRA5, SEMA3C, MFAP2, MTERF2, KDM2B, FOXP2 [85][86][87][88][89][90][91], indicating TQ's potential in targeting key molecular pathways in GBM.…”